The Journal of Neurophysiology Vol. 84 No. 6 December 2000, pp. 3056-3066
Copyright ©2000 by the American Physiological Society

Peptide-Induced Ca²⁺ Movements in a Tonic Insect Muscle: Effects of Proctolin and Periviscerokinin-2

 ¹Department of Zoology, Stockholm University, SE-106 91 Stockholm, Sweden; and  ²Institute of General Zoology and Animal Physiology, Friedrich-Schiller-University, D-07743 Jena, Germany

Wegener, Christian and Dick R. Nässel. Peptide-Induced Ca²⁺ Movements in a Tonic Insect Muscle: Effects of Proctolin and Periviscerokinin-2. J. Neurophysiol. 84: 3056-3066, 2000. Although most of the characterized insect neuropeptides have been detected by their actions on muscle contractions, not much is known about the mechanisms underlying excitation-contraction coupling. Thus we initiated a pharmacological study on the myotropic action of the peptides periviscerokinin-2 (PVK-2) and proctolin on the hyperneural muscle of the cockroach Periplaneta americana. Both peptides required extracellular Ca²⁺ to induce muscle contraction, and a blockage of sarcolemmal Ca²⁺ channels by Mn²⁺ or La³⁺ inhibited myotropic effects. The peptides were able to induce contractions in dependence on the extracellular Ca²⁺ concentration in muscles depolarized with high K⁺ saline. A reduction of extracellular Na⁺, K⁺, or Cl did not effect peptide action. Nifedipine, an L-type Ca²⁺-channel blocker, partially blocked the response to both peptides but to a much lesser extent than contractions evoked by elevated K⁺. Using calcium imaging with fluo-3, we show that proctolin induces an increase of the intracellular Ca²⁺ concentration. In calcium-free saline, no increase of the intracellular Ca²⁺ concentration could be detected. The inhibiting effect of ryanodine, thapsigargin, and TMB-8 on peptide-induced contractions suggests that Ca²⁺ release from the sarcoplasmic reticulum plays a major role during peptide-induced contractions. Preliminary experiments suggest that the peptides do not employ cyclic nucleotides as second messengers, but may activate protein kinase C. Our results indicate that the peptides induce Ca²⁺ influx by an activation or modulation of dihydropyridine-sensitive and voltage-independent sarcolemmal Ca²⁺ channels. Ca²⁺-induced Ca²⁺ release from intracellular stores, but not inositol trisphosphate-induced Ca²⁺ release, seems to account for most of the observed increase in intracellular Ca²⁺. Additionally, both peptides were able to potentiate glutamate-induced contractions at threshold concentrations.